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Dexpanthenol reduces diabetic nephropathy and renal oxidative stress in rats

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Date

2019

Author

Tutun, B.
Elbe, Hülya
Vardı, N.
Parlakpınar, H.
Polat, A.
Günaltılı, M.
Yaşar, E. N.

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Abstract

Hyperglycemia increases reactive oxygen species (ROS) and the resulting oxidative stress contributes to the development of diabetic complications. Dexpanthenol (Dxp) is the biological active form of pantothenic acid. We investigated whether Dxp administration could decrease oxidative stress as a way to treat renal complications of diabetes mellitus (DM). Thirty-two male Wistar albino rats were divided into four groups: control, Dxp, DM and DM + Dxp. Experimental diabetes was induced by a single dose of streptozotocin (STZ). After administration of STZ, the DM + Dxp group was administered 500 mg/kg Dxp intraperitoneally every day for 6 weeks. At the end of the study, blood glucose levels were measured and rats were sacrificed. Kidneys were embedded in paraffin, sectioned and stained with hematoxylin and eosin, and periodic acid-Schiff. The mean malondialdehyde levels, glutathione peroxidase, superoxide dismutase and catalase activities, and total antioxidant and total oxidant status also were measured. The control group was normal in histological appearance. We observed congestion, inflammation, glomerulosclerosis, tubular desquamation, loss of villi and hydropic degeneration in tubule cells in the DM group. Indicators of oxidative stress were elevated and antioxidant activity was reduced in the DM group compared to controls. In the DM + Dxp group, oxidative stress was decreased, antioxidant activity was increased and histopathological changes were reduced compared to the DM group. We found that Dxp exhibited ameliorative effects on STZ induced diabetic nephropathy by increasing antioxidant activity.

Source

Biotechnic & Histochemistry

Volume

94

Issue

2

URI

https://doi.org/10.1080/10520295.2018.1508746
https://hdl.handle.net/20.500.12809/1091

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  • PubMed İndeksli Yayınlar Koleksiyonu [2082]
  • Scopus İndeksli Yayınlar Koleksiyonu [6219]
  • Temel Tıp Bilimleri Bölümü Koleksiyonu [193]
  • WoS İndeksli Yayınlar Koleksiyonu [6466]



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